The following thesis explores the physiological effects on European sea bass (Dicentrarchus labrax) and shore crabs (Carcinus maenas) resulting from the dissolution of anthropogenic carbon dioxide (CO2) into seawater: known as ocean acidification. It assesses how ocean acidification, characterised by elevated seawater pCO2 (1200 µatm) and lowered pH (~7.7), affect the internal chemistry of these animals through the homeostatic process of acid-base regulation. Control conditions used for comparison were close to current ocean average values for CO2 (~400 µatm) and pH (8.2). The proficiency and magnitude of these compensatory mechanisms was explored. Both sea bass and shore crabs were found to be highly effective acid-base regulators and employed the same strategy to compensate the hypercapnia-induced respiratory acidosis: namely an elevation of extracellular bicarbonate (HCO3-). It then considers how these regulatory mechanisms both affect, and are affected by, simultaneous exposure to a ubiquitous coastal metal contaminant, copper. Evidence for a hitherto undocumented protective effect of elevated HCO3- against copper-induced DNA damage was found to be afforded to both sea bass and shore crab cells. DNA damage was used as a sensitive toxicity marker and blood cells were used as proxies for other internal tissues. Erythrocytes exposed in vitro (2 h) to copper (45 µg/L) showed significant DNA damage under control [HCO3-] (6 mM) but were completely protected when exposed under high [HCO3-] (12 mM). A similar protective effect was apparent in crabs under in vivo exposure (14 d) to 10 µg/L waterborne copper. Conversely, during exposure to higher waterborne copper concentrations (sea bass: 80 µg/L, shore crabs: 40 µg/L), animals showed a severe or total inhibition of acid-base regulatory ability in the face of simultaneously elevated seawater CO2 (1200 µatm). The downstream effects of longer-term (28 d) exposure to high CO2 and copper, both individually and in combination was assessed. Food conversion efficiency (FCE), growth and copper accumulation were quantified in juvenile sea bass as economically relevant endpoints. Growth and FCE remained unaffected by either stressor and copper was not accumulated in the muscle tissue: pertinent to human consumption. As a bi-product of this longer term study assessment of gut calcium carbonate production rates in these animals was possible, providing some of the first evidence of excretion rates in fish fed on naturally high calcium diets. A directly proportional influence of feeding rate on gut carbonate excretion rates as a result of increased dietary calcium was observed, and novel evidence provided of the proportional contribution of dietary and seawater calcium to excreted carbonate. Both findings have considerable application to global models of fish contribution to the oceanic carbon cycle.